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PubMed1998

[Significance of systemic inflammation in 1,278 trauma patients].

The association between the increasing severity of systemic inflammatory response syndrome (SIRS) and the incidence of post-traumatic complications and mortality was retrospectively investigated in 1278 injured patients. Patients were divided into three groups according to their Injury Severity Score (ISS) (group A: ISS > or = 9 < or = 16 points (n = 626); group B: ISS > 16 < 40 points (n = 589); group C: ISS > or = 40 points (n = 63). SIRS was defined according to the criteria of the American Consensus Conference. The number of fulfilled criteria determined its severity: moderate SIRS: 2 criteria fulfilled, intermediate SIRS: 3 criteria fulfilled, severe SIRS: 4 criteria fulfilled. Additionally, acute respiratory distress syndrome (ARDS) was defined according to the Murray-Score and the multiple organ dysfunction syndrome (MODS) according to the Goris-Score. The incidence of SIRS was 42% in group A, 70% in group B and 100% in group C (p < 0.05). The severity of SIRS increased with severity of trauma. Moreover, 178 of all injured patients (14%) developed septic complications. In parallel to SIRS, the incidence of these septic complications correlated with the severity of trauma. The occurrence and severity of ARDS and MODS correlated with increased severity of SIRS and septic complications. Among patients without SIRS 15% developed ARDS and 21% MODS. In contrast, patients with severe SIRS and septic complications demonstrated ARDS in 99% and MODS in 97%. In these patients, no correlation was found between the ISS and the incidence of ARDS or MODS. There were also stepwise increases in mortality rates in the hierarchy from SIRS to septic shock. While 13 of patients with modest SIRS (5%) and 32 of patients with intermediate SIRS (13%) died, the mortality rate of patients with severe SIRS was 19% (P < 0.05). In addition, a significant correlation between the incidence of septic complications and mortality was found. Injured patients with sepsis died in 13%, those with severe sepsis in 23%, and patients with septic shock in 33% (p < 0.05). Thus, the increasing severity of SIRS was associated with the occurrence of posttraumatic ARDS, MODS, and mortality. Using the number of fulfilled SIRS criteria for classifying systemic inflammation, its severity may be predictive for posttraumatic complications and outcome of injured patients.

Adult↗

PubMed2002

Systemic inflammation induced by lipopolysaccharide increases neointimal formation after balloon and stent injury in rabbits.

BACKGROUND: Emerging data indicate that the inflammatory response after mechanical arterial injury correlates with the severity of neointimal hyperplasia in animal models and postangioplasty restenosis in humans. The present study was designed to examine whether a nonspecific stimulation of the innate immune system, induced in close temporal proximity to the vascular injury, would modulate the results of the procedure. Methods and Results- Rabbits subjected to iliac artery balloon injury (balloon denudation with or without stent deployment) were injected twice with a bacterial lipopolysaccharide (LPS) (500 ng/rabbit) before and after surgery. The dose was chosen to be sufficient to induce systemic inflammation but not septic shock. A systemic marker of inflammation (serum interleukin-1beta levels measured by ELISA) and monocytic stimulation (CD14 levels on monocytes measured by flow cytometry) were increased after LPS administration. Arterial macrophage infiltration at 7 days after injury was 1.7+/-1.2% of total cells in controls and 4.2+/-1.8% in LPS-treated rabbits (n=4, P<0.05). Morphometric analysis of the injured arteries 4 weeks after injury revealed significantly increased luminal stenosis (38+/-4.2% versus 23+/-2.6, mean+/- SEM; n=8, P<0.05) and neointima-to-media ratio (1.26+/-0.21 versus 0.66+/- 0.09, P<0.05) in LPS-treated animals compared with controls. This effect was abolished by anti-CD14 Ab administration. Serum interleukin-1beta levels and monocyte CD14 expression were significantly increased in correlation with the severity of intimal hyperplasia. LPS treatment increased neointimal area after stenting from 0.57+/-0.07 to 0.77+/- 0.1 mm(2) and stenosis from 9+/-1% to 13+/-1.7% (n=5, P< 0.05). CONCLUSIONS: Nonspecific systemic stimulation of the innate immune system concurrently with arterial vascular injury facilitates neointimal formation, and conditions associated with increased inflammation may increase restenosis.

Angioplasty, Balloon↗

PubMed2004

Low-density lipoprotein triglycerides associated with low-grade systemic inflammation, adhesion molecules, and angiographic coronary artery disease: the Ludwigshafen Risk and Cardiovascular Health study.

BACKGROUND: Markers of systemic inflammation and LDL cholesterol (LDL-C) have been considered independent risk factors of coronary artery disease (CAD). We examined whether alterations of LDL metabolism not reflected by LDL-C were associated with low-grade inflammation, vascular injury, and CAD. METHODS AND RESULTS: We studied 739 subjects with stable angiographic CAD and 570 matched control subjects in which CAD had been ruled out by angiography. The association of LDL triglycerides (LDL-TGs) (odds ratio [OR], 1.30; 95% CI, 1.19 to 1.43; P<0.001) with CAD was stronger than that of LDL-C (OR, 1.10; 95% CI, 1.00 to 1.21; P=0.047). The predictive value of LDL-TG for CAD was independent of LDL-C. "Sensitive" C-reactive protein (CRP), serum amyloid A, fibrinogen, interleukin 6, intercellular adhesion molecule-1 (ICAM-1), and vascular adhesion molecule-1 (VCAM-1) increased in parallel to LDL-TG. CRP, ICAM-1, and VCAM-1 were inversely related to LDL-C. To examine whether LDL-TGs were associated with the distribution of LDL subfractions, we studied 114 individuals with impaired fasting glucose, impaired glucose tolerance, or type 2 diabetes mellitus. In subjects with high LDL-TG, LDLs were depleted of cholesteryl esters (CEs), and VLDLs, IDLs, and dense LDLs were significantly elevated. CONCLUSIONS: Alterations of LDL metabolism characterized by high LDL-TG are related to CAD, systemic low-grade inflammation, and vascular damage. High LDL-TGs are indicative of CE-depleted LDL, elevated IDL, and dense LDL. LDL-TG may better reflect the atherogenic potential of LDL than LDL-C.

Aged↗

PubMed2026

Childhood Economic Mobility and Systemic Inflammation Among Men Who Experienced Low Income in Toddlerhood: The Moderating Role of Trait Hostility.

OBJECTIVE: Childhood economic upward mobility (ie, increases in family income across childhood) may attenuate links between childhood poverty and systemic inflammation in adulthood, the extent of which may vary depending on inter-individual differences in personality characteristics, including hostility. METHODS: Men who experienced low income in toddlerhood (N=171) were followed prospectively into adulthood. Annual family income was collected 12 times when men were 1.5 to 17 years old. Men completed the Cook-Medley Hostility Scale and had their fasting blood drawn to measure circulating levels of C-reactive protein (CRP) at age 32. Multiple linear regression analyses examined main and moderation effects of childhood economic upward mobility and adult hostility on CRP levels adjusting for income at 1.5 years, race, parent educational attainment, and adult income, education, waist circumference, and smoking status. RESULTS: Main effects were nonsignificant, but an interaction effect emerged. Counter to expectations, childhood economic upward mobility related to greater adult CRP as trait hostility decreased ( β =-0.203, P =.018). Simple slope analyses further revealed that childhood economic upward mobility was positively associated with CRP among men lower in hostility ( β =0.23, SE=0.09, P =.020) but was unrelated to CRP among men higher in hostility. Results of post hoc sensitivity analyses are also discussed. CONCLUSIONS: Counterintuitive findings suggest that for men who experience poverty in toddlerhood, the association between childhood economic upward mobility and adult CRP may be nuanced and even in the positive direction for men low in hostility, which aligns with work on unintended health consequences of upward mobility.

Humans↗

PubMed2000

Thermoregulatory manifestations of systemic inflammation: lessons from vagotomy.

The multiple effects of vagotomy on the thermoregulatory response to systemic inflammation are reviewed (primarily, for the model of intravenous lipopolysaccharide administration in the rat). The following conclusions are drawn. (1) Vagotomy-associated thermoeffector insufficiency is likely to account for the attenuation of the fever response observed in some--but not all--studies; such an insufficiency is, however, preventable by postoperative care, including the use of a liquid diet. (2) The febrile response to low doses of lipopolysaccharide (monophasic fever) is mediated by the hepatic (but not gastric or celiac) vagal fibers, presumably afferent; the same fibers are likely to be involved in the development of tolerance to low doses of circulating endotoxins. (3) Phase 1 of the polyphasic febrile response to moderate doses of lipopolysaccharide involves capsaicin-sensitive afferents (either nonvagal only or both nonvagal and vagal), does not involve cholecystokinin A-receptors, and may involve peripheral prostaglandins. (4) Febrile phase 2 does not require the integrity of abdominal nerve fibers, either vagal or nonvagal, at least in the rat. (5) Phase 3 of the febrile response to intravenous lipopolysaccharide (and perhaps the response to intraperitoneal lipopolysaccharide) involves capsaicin-insensitive vagal fibers, presumably efferent; the involvement of these fibers in febrigenic mechanisms is strongly modulated by an unknown factor. (6) A hepatoceliac vagal, presumably efferent, mechanism ('an anti-inflammatory pathway') counteracts the development of lipopolysaccharide-induced hypothermia and shock.

Animals↗

PubMedDate not supplied

Systemic inflammation as a cardiovascular disease risk factor and as a potential target for drug therapy.

Inflammation-related processes play a key role the current etiologic model of atherosclerosis and its acute complications. Recent evidence suggests that blood-based biomarkers that reflect systemic inflammation may contribute to our ability to predict future risk of cardiovascular disease. Global markers of inflammation, such as C-reactive protein and fibrinogen, have been well studied as potential cardiovascular risk factors. A variety of additional markers that reflect various elements of the complex systems governing inflammation, including proinflammatory and antiinflammatory cytokines, mediators of cellular adhesion, and matrix degradation enzymes, are also worthy of study. Although many previous studies have examined the relation of inflammation to myocardial infarction, emerging evidence suggests that other cardiovascular phenotypes such as ischemic stroke and early-stage atherosclerosis may also be related to inflammation. Further elucidating the role of inflammation in cardiovascular disease may lead to the identification of new targets for preventive or therapeutic interventions. In addition, markers of inflammation may be useful as a means to predict or monitor an individual's response to currently available cardiovascular therapies, such as aspirin or HMG coenzyme A reductase inhibitors, that may act via antiinflammatory mechanisms.

Biomarkers↗

PubMed2002

Local and systemic inflammation in patients with chronic obstructive pulmonary disease: soluble tumor necrosis factor receptors are increased in sputum.

Chronic obstructive pulmonary disease (COPD) is characterized by significant chronic inflammation in the pulmonary compartment as well as in the circulation. This study aimed to elucidate the relationship between local and systemic inflammation in smoking-induced COPD by assessing levels of soluble (s) tumor necrosis factor (TNF) receptors, TNF-alpha, and interleukin-8 (IL-8) in induced sputum and in plasma. Sputum induction was performed in 18 subjects with COPD (FEV(1) 56% predicted) and 17 healthy smokers (FEV(1) 99% predicted). Patients with COPD showed significantly higher percentages of neutrophils and levels of sTNF-R55 and IL-8 in sputum as compared with control subjects, whereas sputum sTNF-R75 levels tended to be higher in COPD. Sputum TNF-alpha levels were similar in both groups. When comparing sTNF receptors in sputum and plasma, no direct correlations were found despite elevation of circulating sTNF-R75 levels in patients with COPD. In addition, sputum sTNF receptors were inversely related to the FEV(1) in patients with COPD, whereas circulating sTNF receptors were not, suggesting different regulation of inflammation in the pulmonary and systemic compartment. When subjects were divided according to their current smoking status, levels of sTNF-R55, sTNF-R75, and IL-8 in sputum were significantly elevated in ex-smoking versus currently smoking patients with COPD, suggesting ongoing inflammation in airways and circulation of patients with COPD after smoking cessation.

Aged↗

PubMed2006

Subcutaneous adipose tissue cytokine production is not responsible for the restoration of systemic inflammation markers during weight loss.

CONTEXT: It has been suggested that weight loss can improve systemic inflammation associated with obesity by decreasing the adipose production of pro-inflammatory cytokines. This suggestion, however, remains controversial. OBJECTIVE: To analyse the effect of weight loss on peripheral inflammatory markers and subcutaneous adipocytokine production. DESIGN: Patients were studied at baseline, at the end of the weight loss period, and after 2 weeks of weight stabilisation. SUBJECTS: Nineteen morbid obese non-diabetic patients and 20 lean control subjects. INTERVENTION: During the weight loss period patients followed a 6-week low-calorie diet. MEASUREMENTS: Plasma levels of inflammatory markers, maximal in vitro whole-blood cytokine production, subcutaneous adipose tissue expression and content of several cytokines. RESULTS: Obese subjects had higher circulating levels of C reactive protein (CRP), serum amyloid A (SAA), interleukin IL-6, IL-1 and soluble tumor necrosis factor receptors (sTNFR). Weight loss was associated with a significant decrease in CRP, SAA, leucocytes and plasma IL-6. Maximal in vitro cytokine production of IL-1 and sTNFR1 increased during this period. Weight loss did not induce significant changes in the adipose concentrations of IL-6, IL-1 or sTNF-receptors. However, adipose expression of IL-6, IL-1, TNFalpha, membrane cofactor protein-1 and adiponectin increased at the end of the weight loss period. During weight maintenance, circulating inflammatory parameters increased and in some cases returned to baseline. CONCLUSIONS: A low-calorie diet is associated with an improvement in the systemic inflammatory status. This seems to be due to energy restriction rather than to adipose mass loss, since inflammatory levels return to baseline soon after weight stabilisation. Furthermore, a negative energy balance and fat mobilisation are associated with increased subcutaneous cytokine adipose expression.

Adult↗

PubMed2004

Cerebral vascular and metabolic response to sustained systemic inflammation in ovine traumatic brain injury.

Traumatic brain injury (TBI) is frequently accompanied by a systemic inflammatory response secondary to multiple trauma, shock, or infections. This study investigated the impact of sustained systemic inflammation on cerebral hemodynamics and metabolism in ovine traumatic brain injury. Fifteen sheep were investigated for 14 hours. Head injury was induced with a nonpenetrating stunner in anesthetized, ventilated animals. One group (TBI/Endo, n = 6) subsequently received a continuous endotoxin infusion for 12 hours, whereas a second group (TBI, n = 6) received the carrier. Three instrumented animals served as sham controls. Head impact significantly increased intracranial pressure from 9 +/- 4 mm Hg to 21 +/- 15 mm Hg (TBI/Endo) and from 10 +/- 3 mm Hg to 24 +/- 19 mm Hg (TBI) (means +/- SD). Internal carotid blood flow increased and cerebral vascular resistance decreased (P < 0.05) during the hyperdynamic inflammatory response between 10 and 14 hours in the TBI/Endo group, whereas these parameters were at baseline level in the TBI group. Intracranial pressure remained unchanged during this period, but increased during hypercapnia. The CMRO2, PaCO2, and arterial hematocrit values were identical among the groups between 10 and 14 hours. It is concluded that chronic endotoxemia in ovine traumatic brain injury was associated with cerebral vasodilation uncoupled from global brain metabolism. Different mechanisms appear to induce cerebral vasodilation in response to inflammation and hypercapnia.

Animals↗

PubMed2003

Activity of the hypothalamic-pituitary-adrenocortical system and sleep-wake cycle in rats with acute systemic inflammation.

Activity of the hypothalamic-pituitary-adrenocortical system and EEG characteristics of the sleep-wake cycle were studied on adult male Wistar rats with acute inflammation produced by bacterial lipopolysaccharide in a dose of 250 microg/100 g body weight. Blood concentrations of adrenocorticotropic hormone and corticosterone increased by 6 and 10 times, respectively, 30 min after lipopolysaccharide administration and peaked 2 hours after challenge. In this period the sleep-wake cycle underwent the most pronounced changes that could be attributed to the stupor-like state observed in clinical practice. It was manifested in dissociation between locomotor activity of animals and EEG characteristics, suppression of EEG components in slow-wave sleep, increase in the number of beta-waves, and decrease in the number of delta-waves in EEG. In the present work we consider possible mechanisms of temporal relationships between activity of the hypothalamic-pituitary-adrenocortical system and disorganization of the sleep-wake cycle during acute systemic inflammation.

Adrenocorticotropic Hormone↗

PubMed2002

Hyperzincemia with systemic inflammation: a heritable disorder of calprotectin metabolism with rheumatic manifestations?

A boy had infantile-onset systemic inflammation, growth failure, hepatosplenomegaly, anemia, leukocytopenia, progressive muscular dystrophy, and hypercalprotectinemia, resulting in marked hyperzincemia. His mother had a history of chronic arthritis since childhood and also showed hypercalprotectinemia/hyperzincemia. We postulate an inherent defect in calprotectin metabolism.

Adolescent↗

PubMed1996

Cytokines in stored red blood cell concentrates: promoters of systemic inflammation and simulators of acute transfusion reactions?

BACKGROUND: The cytokine network has important implications for the systemic inflammatory and metabolic response in trauma and infection. Cytokines exogenously administered to traumatized and infected patients may have implications for the trauma response in these patients. The main objective of this study was to characterize red blood cell concentrates (RBCs) with regard to cytokine content. METHODS: We investigated the concentrations of tumor necrosis factor alpha (TNF), interleukin-1 beta (IL-1), interleukin-6 (IL-6) and interleukin-8 (IL-8) in sixteen units of RBCs stored at +4 degrees C during 40 days. Samples from RBCs were taken every tenth day. Healthy volunteers were used as controls. RESULTS: IL-1 and IL-8 in RBCs were increased compared to controls, P < 0.01 - P < 0.001 and TNF in RBCs were increased on days 1 and 40 compared to controls, P < 0.05. During storage TNF was highest on day 1, 69 (< 3-1060) pg/ml, median (range). IL-1 concentrations increased during the period of storage from 5 (< 2 - 205) pg/ml to 174 (< 2 - 2180) pg/ml, P < 0.01. IL-6 was 6 (< 2 - 210) pg/ml on day 1 and did not change over the period of storage. IL-8 was highest on day 40, 164 (15 - 790) pg/ml and compared to day 1 the concentrations were increased on day 10 and day 40, P < 0.05 for both comparisons. CONCLUSIONS: The results indicate the presence of TNF, IL-1, IL-6 and IL-8 in stored RBCs, though there was a great variability over the period of storage and between units of RBCs. In some samples of RBCs the content of cytokines reached levels that may be anticipated to contribute to systemic inflammation and the symptomatology of acute transfusion reactions.

Adult↗

PubMed2004

Periodontitis and systemic inflammation: control of the local infection is associated with a reduction in serum inflammatory markers.

Severe periodontitis is associated with elevated inflammatory markers in otherwise healthy populations. However, the nature of this association has not been determined. Our aim was to assess whether the degree of response to periodontal therapy was associated with changes in serological markers of systemic inflammation. Ninety-four systemically healthy subjects with severe generalized periodontitis participated in a prospective six-month blind intervention trial. Periodontal parameters and inflammatory markers [C-reactive Protein (CRP) and Interleukin-6 (IL-6)] were evaluated prior to and 2 and 6 mos after delivery of standard non-surgical periodontal therapy. Six months after treatment, significant reductions in serum IL-6 (p < 0.001, median decrease 0.2 ng/L, 95% CI 0.1-0.4 ng/L) and CRP (p < 0.0001, median decrease 0.5 mg/L, 95% CI 0.4-0.7) were observed. Decreases in inflammatory markers were significant in subjects with above average clinical response to periodontal therapy after correction for possible confounders. Periodontitis may add to the systemic inflammatory burden of affected individuals.

Aggregatibacter actinomycetemcomitans↗

PubMed2006

Recurrent obstructive apneas trigger early systemic inflammation in a rat model of sleep apnea.

Obstructive sleep apnea (OSA) is associated with vascular disorders possibly due to systemic inflammation. To determine whether repeated episodes of OSA in a rat model lead to endothelial cell activation and systemic leukocyte recruitment in the microcirculation. Three experimental groups (apnea, sham and naive) were studied. The apnea group was instrumented and subjected to repeated obstruction for 3h (rate 60/h, length 5s) using a special device. The sham group was only instrumented and the naive group was used as a control. Leukocyte-endothelial cell interactions (intravital microscopy) and expression of P-selectin (immunohistochemistry) were determined in colonic venules. The apnea group induced a significant increase in the flux of leukocytes rolling, number of rolling leukocytes and number of adherent leukocytes when compared with the sham or naive groups. P-selectin was up-regulated only in the apnea group. This experimental model of recurrent obstruction demonstrates rapid endothelial cell activation, suggesting the onset of an inflammatory response.

Airway Obstruction↗

PubMed2003

Influence of systemic inflammation on efficiency of antiplatelet therapy in PAOD patients.

Recently it was shown that inflammation adversely influences results obtained from the platelet function analyzer system, PFA-100, hypothesizing that inflammation could confound interpretation of platelet function results. We investigated the clinical relevance of these results in patients with peripheral arterial occlusive disease (PAOD), with and without signs of systemic inflammation. In 98 PAOD patients, all treated with acetyl-salicylic acid (ASA), we obtained PFA-100 values upon stimulation with epinephrine. C-reactive protein (CRP) values were investigated as indicator for systemic inflammation. Mean CRP levels were elevated in 23 patients (23%). There was no difference of mean PFA-100 results between patients with elevated CRP levels and those without. Our results indicate that the effect of ASA on platelet aggregation, as measured by the PFA-100, is not relevantly influenced in PAOD patients with elevated CRP.

Arterial Occlusive Diseases↗

PubMed2002

[Effect of rhubarb on inflammatory cytokines and complements in patients with systemic inflammation reaction syndrome and its significance].

OBJECTIVE: To study the effect of rhubarb in treating patients with systemic inflammation reaction syndrome (SIRS) and its mechanism. METHODS: The 40 patients with SIRS in the treated group were treated with conventional treatment plus rhubarb powder orally or by nasal feeding, the 38 patients in the control group were treated with conventional treatment alone. Serum tumor necrosis factor-alpha (TNF-alpha) was determined by ELISA during the admission and the 3rd day after admission, C-reactive protein (C-RP), complement 3 and 4 (C3, C4) were also determined by auto-scattering turbidimetric quantitative analysis. The parameters were compared between groups and with normal control group. RESULTS: Cure rate in the treated group was significantly higher than that in the control group accompanied with lesser occurrence of multiple organ dysfunction syndrome (MODS) and lower mortality. Serum TNF-alpha, C-RP, C3 and C4 in the SIRS patients were increased during admission, which were significantly higher than normal control, but these parameters would be reduced together with the alleviating of symptoms after treatment, particularly after rhubarb treatment. CONCLUSION: Rhubarb could improve the prognosis of patients with SIRS, its major mechanism is that rhubarb has the antagonizing effect against inflammatory cytokines and complements.

C-Reactive Protein↗

PubMed2000

Systemic inflammation in hemorrhagic fever with renal syndrome correlates with hypotension and thrombocytopenia but not with renal injury.

Systemic inflammation is common in patients with nephropathia epidemica (NE), a European form of hemorrhagic fever. Markers of inflammation were studied in a patient with NE with respiratory insufficiency (patient 1), 18 other patients with NE, and 13 patients with a viral infectious disease other than NE. Neutrophil and monocyte CD11b expression levels, determined by flow cytometry; soluble interleukin (IL)-2 receptor (sIL-2R), IL-6, and IL-8 concentrations, determined by means of Immulite; and soluble E-selectin, determined by ELISA, were higher in patients with NE than in healthy subjects. The findings were not specific for NE and did not correlate with serum creatinine levels, but the findings correlated inversely with mean arterial pressure (sIL-2R and monocyte CD11b expression) and minimum platelet count (sIL-2R, IL-6, neutrophil, and monocyte CD11b expression). Monocyte CD11b expression in patient 1 was extremely high, suggesting that monocytes may contribute to development of lung injury. Severity of inflammation in patients with NE is related to hypotension and platelet consumption but not to renal injury.

Adolescent↗

PubMed2002

Systemic inflammation and innate immune response in patients with previous anterior uveitis.

AIM: To determine the presence of systemic inflammation and innate immune responsiveness of patients with a history of acute anterior uveitis but no signs of ocular inflammation at the time of recruitment. METHODS: Tumour necrosis factor alpha (TNF-alpha) production in response to bacterial lipopolysaccharide (LPS) was studied using whole blood culture assay; levels of TNF-alpha in culture supernatants, and soluble interleukin 2 receptor (sIL-2R) in serum were determined by chemiluminescent immunoassay (Immulite); monocyte surface expression of CD11b, CD14, and CD16 and the proportion of monocyte subsets CD14(bright)CD16(-) and CD14(dim)CD16(+) were studied with three colour whole blood flow cytometry; and serum C reactive protein (CRP) levels were determined using immunonephelometric high sensitivity CRP assay. RESULTS: The CRP level (median, interquartile range) was significantly higher in 56 patients with previous uveitis than in 37 controls (1.59 (0.63 to 3.47) microg/ml v 0.81 (0.32 to 2.09) microg/ml; p=0.008). The TNF-alpha concentration of the culture media per 10(5) monocytes was significantly higher in the patient group than in the control group in the presence of LPS 10 ng/ml (1473 (1193 to 2024) pg/ml v 1320 (935 to 1555) pg/ml; p=0.012) and LPS 1000 ng/ml (3280 (2709 to 4418) pg/ml v 2910 (2313 to 3358) pg/ml; p=0.011). The background TNF-alpha release into the culture media was low in both groups. CD14 expression of CD14(bright)CD16(-) monocytes, defined as antibody binding capacity (ABC), was similar for the patients and controls (22,839 (21,038 to 26,020) ABC v 21,657 (19,854 to 25,646) ABC). CONCLUSIONS: Patients with previous acute anterior uveitis show high innate immune responsiveness that may play a part in the development of ocular inflammation.

Adult↗